The document discusses sino-nasal polyposis, detailing the characteristics, history, epidemiology, and associated diseases of nasal polyps. It presents different theories of their pathogenesis, highlights the role of eosinophils in the condition, and describes macroscopic and microscopic features of polyps. Additionally, it outlines the correlation of nasal polyps with various disorders including cystic fibrosis, asthma, and allergic reactions.

1. Sino-Nasal polyposis
Presenter: Dr. Pradip Mallik
Moderator: Prof. Th Sudhiranjan
Department of Otorhinolaryngology
Regional Institute of medical sciences, Imphal
Dated: 5.3.2013

2. Introduction
• A polyp presents in the nasal cavity with a
grape-like appearance, having a 'body' and a
'stalk'. The surface is smooth and the color is
more yellow than the pink mucous membrane.
• Nasal polyps originate in the upper part of the
nose around the openings to the ethmoidal
sinuses.

3. • Broadly defined, nasal polyps
are abnormal lesions that
originate from any portion of
the nasal mucosa or paranasal
sinuses.
• Polyps are an end result of
varying disease processes in
the nasal cavities.
•
The most commonly
discussed polyps are benign
semitransparent nasal lesions
that arise from the mucosa of
the nasal cavity or from one or
more of the paranasal
sinuses, often at the outflow
tract of the sinuses.

4. History of Nasal polyposis
• The earliest record of nasal polyps is found in
Egyptian literature of approximately 2,000 years bc.
• Hippocrates (460–370 bce) referred to the “nasal
growths” as “polypus” due to their resemblance to the
sea-polyp, and this name has persisted to this day.
• Boerhaave, in 1744, was among the first to surmise
that these growths resulted from elongation of the
linings of the sinus membranes.

5. • In 1843, Frerichs and Billroth proposed that polyps
were truly a hypertrophy of normal Sino nasal
mucosa, as the epithelium covering the polyp was
similar to the mucosa of the originating sinus.
• Advances in immunohistochemistry and
immunobiology in the 1940s led to the first description
of the predominance of eosinophil and lymphocyte
populations in polyps.
• Messerklinger’s discoveries, functional endoscopic
sinus surgery (FESS) was introduced in the late 1960s
in Germany, and David Kennedy is credited for
introducing FESS in the United States in 1985.

6. EPIDEMIOLOGY
• The prevalence of nasal polyps (NP) in the population has been
grossly estimated as 1–4%.
• It increases with age, reaching a peak in those aged 50 years and
older.
• Male: Female = 2:1
• An association between NP and allergic rhinitis (AR) is weak, with
NP prevalence in patients with AR estimated between 1.5 and 1.7%
and this incidence is similar to that of the general population.
• Nasal polyposis occurs with a high frequency in groups of patients
having specific airway diseases

7. Disease
Group
Percentage
Allergic Rhinitis
In Adult
0.1
In children
1.5
Non-allergic Rhinitis
Asthma in adults
5
Allergic
5
Non-allergic
13
NSAID intolerance
36-72
NSAID intolerance+asthma
80
Allergic fungal
rhinosinusitis
>80
Churg-strauss syndrome
50
Cystic fibrosis
10
In adults
Primary ciliary dyskinesia
In children
40
40

8. • Genetic inheritance has been proposed as a
possible etiology of NP. Studies have
suggested that up to 14% of patients with NP
have a family history of NP.
• In a Caucasian population, NP have been
shown to have a strong eosinophilic
component while NP in Asian countries show a
neutrophilic pattern.
• Up to 80% of NSAID insensitive patients have
NP.

9. ETIOLOGY and ASSOCIATED
DISEASES
• The aspirin triad: A triad of nasal
polyposis, aspirin and asthma was described
(Samtard’s triad) and it represents the most
aggressive forms of disease.
• It is a nonallergic entity and the intolerance is
not confined to acetylsalicylic acid, as the
patients react to other NSAIDs.

10. ALLERGY?
• It was believed that allergy is a significant cause of nasal
polyposis as most of the polyps are characterized by
tissue eosinophilia.
• Most studies have failed to show a higher occurrence of
positive skin tests to inhaled allergens in patients with
polyps than in the general population.
• According to Keith et al there is no deterioration of nasal
symptoms or eosinophilia during the pollen season in
polyp patients having a positive skin test to pollen.
Thus, it appears that allergy is not a well documented
cause or aggravating factor in nasal polyposis.

11. Cystic fibrosis:
• Cystic fibrosis (CF), also known as mucoviscidosis, is an autosomal
recessive genetic disorder that affects most critically the lungs, and
also the pancreas, liver, and intestine.
•
It is characterized by abnormal transport of chloride and sodium
across an epithelium, leading to thick, viscous secretions.
• Nasal endoscopy demonstated polyp in 45% of adults with cystic
fibrosis.
•
Mucosal abnormalities in the sinuses consistent with polypoid
hyperplasia are demonstrated on computed tomography (CT) scans
in almost all patients with CF.
• A sweat chloride test is recommended in any child with nasal
polyps, to rule out cystic fibrosis.

12. Kartagener’s syndrome:
• Primary ciliary dyskinesia (PCD), also known as
immotile ciliary syndrome.
• Rare, ciliopathic, autosomal recessive genetic disorder.
• It causes a defect in the action of the cilia lining the
respiratory tract (lower and upper, sinuses, Eustachian
tube, middle ear) and fallopian tube, and also of the
flagella of sperm in males.
• Absent mucociliary clearance and recurrent bacterial
infections result in nasal polyposis in about 40 percent
of the patients. The recurrence rate is low after surgery.

13. Young syndrome
• It is a rare condition which consists of
recurrent respiratory disease with
• Chronic rhinosinusitis,
• Nasal polyps,
• Bronchiectasis and
• Azoospermia.

14. Pathogenesis & Pathophysiology
• The pathogenesis of nasal polyps explains how the
polyps start and grow.
• The pathophysiology of nasal polyps explains the
events and processes taking place in the outgrowth of
nasal polyps.
• Several pathogenetic theories on the formation of nasal
polyps have been published during the last 150 years
that have been summarised previously These theories
are based on oedema, an increase in tubulo-alveolar
glands, the presence of the cysts of mucous glands and
on mucous glands of NP.

15. Adenoma and fibroma theory
• Billroth found increased number of long tubulous glands in the polyps.
• The NP were interpreted as adenomas that began by growing under the
nasal mucosa, pushing the epithelium and the original nasal glands
outwards.
•
Hopmann did not find any glands in the NP from his study and interpreted
NP as soft fibromas, protruding towards the nasal mucosa.

16. Necrotizing Ethmoiditis Theory
• This theory supposes that ethmoiditis leads to periostitis and
osteitis of the ethmoid bone and causes bone necrosis.
• Hayek argued strongly against this theory, based on the fact
that he could not found bone necrosis in the ethmoid sinus.

17. Glandular-Cyst Theory
• This theory is based upon the presence of cystic glands and mucusfilled cysts in NP.
• It is hypothesised that oedema of the nasal mucosa causes
obstruction of the ducts of basal glands, leading to the formation of
cysts in the nasal mucosa.
• The cysts expand and push the nasal mucosa downwards, forming a
polyp.

18. Mucosal Exudate Theory
• Hayek believed that the formation of NP
started via an exudate localised deep in the
nasal mucosa, which pressed outwards
caudally.
• According to this theory, both layers of the
tubulo-alveolar sero-mucous nasal glands
should be displaced outwards and be found in
the distal part of the polyp.

19. Theory on Cystic Dilatation
of the Excretory Duct of Nasal
Glands and Vessel Obstruction
• According to this theory in chronic inflammation of the nasal
mucosa, excretory ducts of nasal tubulo-alveolar glands are
obstructed, distended and dilated into cystic structures.
• The capillaries and veins (which are arranged around the
excretory ducts and the gland mass) become stretched and
obstructed, resulting in increased permeability, transudation
and oedema.
• This theory has been used to explain polyp formation in cystic
fibrosis.

20. Blockade Theory
• The theory of Jenkins is based on the premise that
the polyp formation is always preceded by the
same degree of chronic inflammation, either
infectious or allergic.
• The polyp itself is an accumulation of
intercellular fluid dammed up in a localised
tissue.
• The dam is usually caused by an infiltration of
round cells, producing blockade of intercellular
spaces and local lymph oedema.

21. Peri-Phlebitis and PeriLymphangitis Theory
• The theory of Eggston and Wolff is based upon the
recurrent infections that lead to the blocking of
intercellular fluid transport in the mucosa and oedema
of the lamina propria.
• If the oedema involves major areas, the result is the
prolapse of the mucosa and formation of polyps.

22. Glandular Hyperplasia Theory
• Krajina found in cases of chronic infection or allergy
localised infiltrates in the nasal mucosa and localised
hyperplasia of nasal glands.
• The glands will increase in size and cause bulging of
the mucosa.

23. Epithelial Rupture Theory
• In the initial stage of polyp
formation, an epithelial
rupture or necrosis caused
by inflammation and tissue
pressure from the
oedematous and infiltrated
lamina propria takes place.
• Lamina propria protrudes
through the epithelial
defect, and the adjacent
epithelium tends to cover
the defect by migrating
from the surroundings.

24. • If the epithelial defect
is not covered soon
enough or if it is
insufficiently covered,
the prolapsed lamina
propria continues to
grow and the polyp,
with its vascular stalk,
is established.
• After epithelialization
of the polyp, the
characteristic new, long
tubulous glands are
formed

25. Mucous gland in nasal polyp
• In most of the pathogenetic theories, the mucous glands have played a role.
• The glandular orifices are irregularly distributed, as there is no particular
concentration of glands in the stalk or in the most distal end of the polyp.
• The density of glands in NP is considerably lower than in the nasal mucosa.
• The polyp glands are tubular, of different shapes and sizes and differ widely
from those of the nasal glands.
• The most striking glands are the long tubular glands, which may be 1–8 mm of
length.
• Some are very simple, narrow tubes other have prominences of small, round,
alveolar bulges on their sides.

26. Long, simple tubular
glands (a, f).
Long tubular
glands with some branches
(b–e).
Short, simple tubular
glands (g).
Short, branched
tubular glands (h, i).
Tubular glands with
flask-shaped dilatation
(j, k).
Tubulo-alveolar
glands, which are found
extremely rarely (l)

27. Cellular Infiltration
• Eosinophilic inflammation is an important feature in the
pathogenesis of chronic Rhinosinusitis (CRS) with nasal polyps.
• The eosinophilic accumulation in the polyp stroma is basically
caused by increased transendothelial migration and increased
survival time in the tissue, where an increased concentration of
interleukine 5 (IL-5) plays a major role.
• The increased amount of IL-5 is predominantly released from Tlymphocytes, independently of atopy, and the highest concentration
has been found in polyps from patients with non-allergic asthma and
acetylsalicylic acid (ASA) intolerance.
• These are the sub-groups of patients also known to exhibit the
greatest accumulation of eosinophils

28. • In the ASA intolerant patients, a lowered
prostaglandin E2 (PGE2) production has been
observed.
• PGE2 has a significant anti-inflammatory
activity, including inhibition of eosinophils.
• A possible intrinsic defect in PGE2 production
might, therefore, be responsible for a further
increase of eosinophilic accumulation in ASA
intolerant patients.

29. Role of Staphylococcus aureus
enterotoxins (SAE)
• Multiclonal IgE antibody formation to SAE
can be seen in nasal polyp tissue, but rarely in
CRS.
• It is positive in about 30-50% of the patients
with NP and in about 60-80% of nasal polyp
subjects with asthma

30. Nasal polyposis: aetiology and pathogenesis
Epithelial damage (barrier
dysfunction)
chronic microbial trigger
B
T
Hyper IgE
Cytokines
Polyclonal IgE
Albumin
Superantigens
S. Aureus enterotoxins: disease modifiers
Eosinophils
( apoptosis)
IL-5
Chemokines
Eotaxin
ECP

31. Demo for Pathogenesis
polyps
Mast cell
eosinophil
Arachydonic acid
Cycloxygenase
Prostaglandin
5 lipoxygenase
Leukotrienes
Histamine
Interleukin
Thanks from Dr. R. Cathcart for this demo
cytokines
B cell

32. Histopathology
Macroscopic:
• Macroscopically, most polyps have an edematous, smooth and shiny
appearance with a soft consistency compared with the surrounding
nonpolypoid mucosa.
• The cut surface is usually pale, edematous with a translucent appearance.
• Polyps are generally mobile and often attached via a stalk to the underlying
mucosa.
• Polyps commonly arise from the middle meatus and the sphenoethmoidal
recess and are often bilateral. However, unilateral polyps are not
uncommon.
• In long-standing polyps, the sinonasal bones may remodel and cause
broadening of the nasal dorsum.

33. • A polyp arising from the maxillary sinus and into
the nasal cavity is characteristic of antrochoanal
polyp and is generally unilateral.
• A proportion of CRS with nasal polyps also has
characteristic thick, dark, and tenacious mucus,
termed eosinophilic mucus.
• This mucus is typically seen in allergic fungal
sinusitis but is also present in patients with severe
and recalcitrant polypoid CRS including cystic
fibrosis and Sampter’s triad and in the lungs of
allergic bronchopulmonary aspergillosis.

34. Macroscopic
appearance of a serially
sectioned edematous polyp
showing a delicate glistening
yellow cut surface

35. • Microscopic:
The major histological characteristics of nasal polyps and
CRS mucosa compared with normal mucosa include
(1) Structural changes involving the epithelium,
submucosa, and sometimes underlying bone; and
(2) The nature and degree of inflammatory cell infiltrate.
Polyps have historically been classified based on their
histological structural appearance and the nature of
predominant inflammatory cell population into 3 types.

36. (1) edematous, eosinophilic, or “ allergic” polyps:
• . Edematous and eosinophilic polyps are the most common type and are
also known as “allergic” nasal polyps.
• These polyps are lined with respiratory epithelium with a range of mucosal
alterations that include ulceration, granulation tissue, acute mucositis,
epithelial and goblet cell hyperplasia, and squamous metaplasia.
• The basement membrane is often thickened, and there is abundant
submucosal edema.
• Mucus retention cysts are common and varying amounts of mixed
inflammatory cell infiltrates contain mostly eosinophils, plasma cells, and
scattered lymphocytes.
• The edematous and eosinophilic polyps are seen in the whole spectrum of
associated disorders including, EMCRS, allergic fungal sinusitis, Sampter’s
triad, cystic fibrosis, and Churg–Strauss syndrome.

37. 1.Edematous polyp
2. thickened
basement membranes
(arrows)
3.marked
submucosal edema resulting
in extensive clear space
between submucosal
connective tissue fibers.
4.scattered
throughout are mixed
inflammatory infiltrates
including eosinophils and
plasma cells

38. • 2. Chronic inflammatory polyp:
• This type is less common, forming less than 10% of inflammatory
nasal polyps.
• These may represent a spectrum of edematous polyps, where
occasionally, when a polyp is traumatized, the stroma may undergo
secondary inflammatory change resulting in a myofibroblastic
proliferation that may mimic a soft tissue neoplasm.
• The main histological features are the presence of submucosal
fibrosis and an often prominent mixed inflammatory infiltrate with a
lymphoid predominance often with germinal centers.
• The surface epithelium is likely to show squamous metaplasia as a
marker of chronicity.

39. 1.Chronic inflammatory
changes in polyps.
2.This polyp
shows an exuberant lymphoid
hyperplasia with reactive
germinal centers.

40. 3) Seromucinous, glandular polyps:
• Polyps with hyperplasia of seromucinous
glands are less common.
• Lesions in this category are relatively new and
somewhat controversial as to their relationship
with true epithelial neoplasms, and include
respiratory epithelial adenomatoid hamartoma
and seromucinous hamartoma.

41. Mucus Histopathology, Including
“Eosinophilic Mucus”
• Secretions from CRS with polyps generally contain more
eosinophils than those without polyps, regardless of
consistency of the mucus.
• Secretions are typically thick, almost solid.
• Stained sections of this mucus typically show clusters of
eosinophils, eosinophil breakdown products (Charcot–
Leyden crystals), and other inflammatory and epithelial
cells.
• This mucus, termed eosinophilic mucus, is the diagnostic
criteria for EMCRS and allergic fungal sinusitis.

42. Antrochoanal polyp
• Antrochoanal polyps are the most common type of choanal polyp.
• Other sites of origin may be sphenoid, ethmoid, rarely septum, and
inferior turbinate.
• Antrochoanal polyps represent 4–6% of all polyps, and in the
pediatric population, up to 33%.
• They have an antral and choanal component. These typically arise
from the posterior wall of maxillary antrum and often have a thin
“neck” that passes through the maxillary sinus ostium (or accessory
ostium).
• They are often unilateral, but may be bilateral on rare occasions.

43. • Macroscopically, these range from erythematous to
cystic with the latter often seen in the antral portion.
• Microscopically, these polyps are lined by ciliated
pseudostratified epithelium that is usually intact, with a
thin basement membrane.
• Stroma may exhibit myxoid change and stromal giant
cells, but usually lacks a significant inflammatory
component.
• Rarely, degenerative changes including cholesterol
granulomas and angiomatous change may be found.

44. Clinical presentation
• Small polyps may not produce symptoms and
may be identified only during routine
examination.
• Small polyps in middle meatus may produce
symptoms and block the outflow tract of the
sinuses causing chronic or recurrent sinusitis
symptoms.

45. Symptom-producing polyps can cause:
•
•
•
•
•
•
•
1) Nasal airway obstruction
2) Post nasal drainage
3) Dull headache
4) Snoring
5) Rhinorrhoea
6) Hyposmia/anosmia
7) Epistaxis if preset may give suspicion of
more serious nasal cavity lesions.

46. • Massive polyposis or a single large polyp (eg:
antrochoanal polyp) can cause:
• 1) Obstructive sleep symptoms
• 2) Chronic mouth breathing
• 3) Altered craniofacial structure.
(Frog face)
• 4) Proptosis
• 5) Hypertelorism
• 6) Diplopia

47. Diagnosis and scoring
• Rhinoscopy: Large polyp can be identified by
anterior rhinoscopy.
• In contrast to hyperplastic turbinate, a polyp can
be made to move by touching with a probe.
• Seen as multiple glistening, grayish white, smooth
pedunculated mass in both side of nasal cavity.
• On probing insensitive to touch, do not bleed and
probe can be passed all around the masses.

48. • Direct nasal endoscopy:
- Preferred method of examination.
- Can diagnose small polyp in middle meatus.
- It gives superior assessment of the extent of
the disease and anatomical abnormalities

49. • Polyp grading system. ( Meltzer et al)
Endoscopic appearance
Score
no visible NP
0
small amount of polypoid
disease confined within
the middle
meatus
1
multiple polyps
occupying the middle
meatus
2
polyps
extending beyond the
middle meatus
3
polyps completely
obstructing the nasal
cavity
4

50. Imaging modalities
• ›› CT scan is the primary modality used to evaluate patients with
NP, but MRI does have an occasional role.
• ›› Conventional radiographs are no longer within the standard of
care for the evaluation of the paranasal sinuses.
• ›› Modern helical multislice CT scanners can produce reconstructed
images of diagnostic quality in any plane of imaging.
• ›› Cystic fibrosis patients have preferential opacification of the
paranasal sinuses, whereas non-CF patients with NP have
preferential opacification of the nasal cavity.
• ›› On MRI, fungal infection may have very low signal on T2weighted images, and may thus mimic aerated sinuses.

51. • Polyps appear radiographically as rounded nodules of soft
tissue along the mucosal surfaces of the paranasal sinuses and
nasal cavity.
• More radiodense than the surrounding mucosal thickening or
secretions, which make them appear slightly brighter on CT.
• This pattern may be reversed if the secretions become
inspissated.

52. • Polyps do not erode into the surrounding bone, but pressure
from a polyp may produce a benign local remodeling pattern
that scallops the underlying bone. (Fig 1)
• This bone remodeling will occasionally thin bony septations
beyond the resolution of CT, giving the appearance of bone
erosion, particularly in the ethmoid septations. (Fig 2)
Fig 1
Fig 2

53. • In antronasal polyps sometimes, the polyp will be narrowed as
it passes through the maxillary os, resulting in a dumbbell
configuration on coronal CT. The medial wall of the maxillary
sinus is usually bowed into the nasal cavity. (Fig 1)
• In antrochoanal polyp the most helpful radiologic feature is the
mass itself extending into the nasopharynx. (Fig 2)
Fig 1
Fig 2

54. • Inflammatory NP is frequently solitary, multiple sinonasal
polyps can occur outside the setting of true NP.
• Complete pansinus opacification is more suggestive of NP.
• CT-scan staging:
Right
Left
Maxillary
0-2
0-2
Ant. Ethmoid
0-2
0-2
Post. Ethmoid
0-2
0-2
Sphenoid
0-2
0-2
Frontal
0-2
0-2
OMC
0/2
0/2
Total
0-12
0-12
0- No opacity
1- Some opacity
2- Total opacity

55. • Middle meatus syndrome. (Fig 1)
• A chronically obstructed sinus may form a mucocele. On CT,
the affected sinus enlarges and its walls become rounded
outward. ( Fig 2)
Fig 1
Fig 2

56. • Allergic fungal sinusitis (AFS). On CT, the presence of hyperdense
secretions between layers of thickened, hypodense mucosa is suggestive of
AFS. (Fig 1)
• Inverted papillomas are often indistinguishable from polyps
radiographically. A lobular (“cerebriform”) configuration is also suggestive
of papilloma. Bony sclerosis and osteoneogenesis are frequently present at
the site of attachment of inverted papillomas. (Fig 2)
Fig 1
Fig 2

57. Laboratory Investigations
• Routine blood examination.
• Serological radioallergosorbent test (RAST) .
• Allergic skin testing for those who are having polyp associated with
allergic rhinitis.
• Sweat chloride test/ genetic testing for custic fibrosis in any child
with multiple benign nasal polyp.
• Nasal smear eosinophils may differentiate allergic from nonallergic
sinus diseases.
• Biopsy from the polyp after evaluation by CT scan/MRI.

58. Histologic finding
NPs are characterised by
• Pseudostratified ciliated columnar epithalium
• Thickening of epithelial basement membrane
• Stroma of NP is oedematous
• Vascularization is poor and lacks innervation
• Hyperplasia of seromucous gland when
comparing with inferior or middle turbinate.

59. • Eosinophils are most commonly found
inflammatory cell in NP (found in 80-90% of
polyps)
• Another inflammatory cell, neutroophil, occurs
in 7% cases. This type of NP associates with
CF, primary ciliary dyskinesia or Young
syndrome.

60. Chemical mediators:
1) Cytokines: IL-1, Il-5 are found regularly
2) Growth factors:
•
•
•
•
•
•
•
TNF:
Alpha and beta found regularly
GM-CSF:
Never – Intermittent
Platelet derived factorpresent
Vascular permeable factors:
Present
Vascular endothelial growth factor:
Present
Insulin like growth factor 1:
Present
Stem cell factor :
Present

61. Immunoglobulins:
•
•
•
•
•
IgG = Same level as MT or IT
IgA = Increased
IgM = Same
IgD = Same
IgE = Increased
Adhesion molecule:
• Vascular adhesion molecule: Present
• E & P selectin : Present

62. Treatment
• Treatment can either be medical and/or surgical.
• Oral and topical nasal steroid administration is the
primary medical therapy.
• Antihistamines, decongestants provide little benefit.
• Immunotherapy is useful in treating associated allergic
rhinitis.
• Antibiotic for bacterial super infections.

63. Intranasal corticosteroids
• Normally used intranasal steroids are Beclomethasone,
Ciclesonide, Flunisolide, Fluticasone Propionate,
Fluticasone furoate, Mometasone furoate,
Triamcinolone Acetonide.
•
•
•
•
•
•
•
They help in:
Reducing polyp size
Increase nasal patency
Reduction in rhinitis symptoms
Reduction in loss of sense of smell
Reduction in recurrence of polyp
Safety

64. Sideeffect of IntraNasal steroids
• - Excoriation and bleeding( can be reduced by
cross hand technique)
• - Beclomethasone dipropionate nasal spray is
associated with the onset of increased
intraocular pressure.
• -Delay in growth in prepubescent children has
led to an FDA warning on all INS

65. Systemic Corrticosteroids
• Can be given as tablets and depot-injections.
• Oral prednisolone can be given at 25mg/daily
for 10-14 days.
• As a depot-injection corresponds 100mg
prednisolone.
• It may serve as medical polypectomy.

66. Risks of systemic steroid
•
•
•
•
•
•
•
Insomnia,
personality change,
truncal obesity,
weight gain,
glaucoma,
cataracts,
osteoporosis (requires greater than 3 months
usage),
• peptic ulcer disease, and
• increased incidence of infection

67. EPOS
2007

68. Surgical Management
General principles surgery for nasal polyposis:
• Selection of the patient who has exhausted medical
management and remains symptomatic.
• The patient must understand the absolute necessity of often
prolonged postoperative care.
• Selection of appropriate anesthetic method and preparation
of the surgical field to maximize visualization and minimize
bleeding.
• Accurate identification of surgical landmarks such as the
lamina papyracea, anterior ethmoid artery, and skull base on
preoperative CT imaging.

69. • Use of stereotactic image-guided surgery when
necessary to confirm the skull base, cribriform
plate, and lamina papyracea.
• Atraumatic removal of polyps and diseased bone
while preserving as much mucosa as possible.
Meticulous removal of osteitic bone and bony
partitions.
• Ongoing postoperative medical management to
prevent disease recurrence.

70. FESS
• Preoperative evaluation by radiology and endoscopic
examination.
• Preoperatively, patients with evidence of active infections
should be administered culture-directed antibiotics to help
eradicate infection and to decrease mucosal inflammation.
• Administration of preoperative oral corticosteroid reduces
the size of the polyp helps in proper visualization.
• Intravenous anesthesia with remifentanil and
propofol, improved visual field with decreased blood loss
has been demonstrated.

71. Steps
• Polyps obstructing the nasal cavity or emanating from the middle meatus
are best addressed with the microdebrider.
• The maxillary sinus is best addressed with 0 and 30 endoscopes.
• Uncinate process is removed with sickle knife, backbiting forcep &
microdebrider.
• The natural ostium of the maxillary sinus should be probed and widened
and that any surgically created ostium is brought into continuity with the
natural as in order to prevent recirculation of mucus.
• In the case of polyposis, large antrostomies are recommended. The sinus
should be inspected with at minimum the 45 endoscope; a 70 endoscope
is advised for analyzing the floor and anterior-most portions of the
maxillary sinus to inspect for polyps and any infraorbital ethmoid cells that
may obstruct the ostium. Inspissated secretions need to be
evacuated, cultured, and sent to pathology for analysis of possible fungal

72. • Anterior ethmoid cells should be meticulously dissected using
through-cutting instruments and polypoid debris removed with the
microdebrider.
• The first important landmark to identify is the medial orbital wall
and the dissection is continued along the medial orbital wall rather
than medially, because the skull base is significantly thicker and less
likely to be injured laterally as opposed to medially where it slopes
down into the middle turbinate.
• It is imperative that foci of ostetic bone along the lamina papyracea
and middle turbinate be removed to help reduce inflammation and
prevent polyp recurrence in these areas.
• Once the basal lamella is identified, the posterior ethmoid cells
should be dissected in a similar fashion.
•
Dissection of the ethmoid cavity typically occurs in an anterior to
posterior fashion, identifying landmarks along the lamina papyracea
and skull base until the anterior face of the sphenoid is encountered.

73. • The superior turbinate is next identified in order to enter the
sphenoid sinus through the sphenoethmoidal recess and its natural
ostium.
• Sinus is entered away from critical structures such as the carotid
artery (dehiscent in up to 20% of cases) and the optic nerve
(dehiscent in 5–10% of cases)
• This method also ensures that a sphenoethmoidal (Onodi) cell is not
mistakenly treated as the sphenoid sinus.
• The sphenoid sinus should be opened widely from the skull base to
lamina papyracea; care must be taken to avoid the septal branch of
the sphenopalatine artery during this dissection.
• Polyps in sphenoid sinus is seen rarely

74. • Once the sphenoid sinus is opened, dissection along
the skull base occurs in a retrograde fashion in order
to clear lamella along the skull base until the frontal
recess is encountered.
• The region of the anterior ethmoid artery is identified
and avoided. It typically lies at the uppermost limit of
the anterior wall of the ethmoidal bulla.
• If an injury to the anterior ethmoid artery occurs,
bipolar electrocautery is used to coagulate the vessel.

75. • Frontal sinus is infrequently diseased with polyps; however, the
frontal recess can be extensively diseased with polyps, resulting in
obstruction of the frontal sinus itself.
• Much of the dissection involves angled instruments and endoscopes.
• In this region, preoperative review of the CT scans is critical, as a
variety of drainage pathways may lead to the frontal sinus and a
ethmoid air cells may invade the frontal sinus, complicating its
anatomy and dissection, and polyps within the frontal recess can
impair vision of these anomalies.
• Through-cutting instruments are used to dissect the anterior ethmoid
lamella until the skull base is skeletonized and the anterior ethmoid
artery identified, just posterior to the frontal recess.
• Partitions separating the frontal sinus from the supraorbital ethmoid
cells are then taken down meticulously. The agger nasi cap is
identified, resected, and frontal recess evaluated.

76. • After a complete dissection of the paranasal sinuses
has been performed, the field should be inspected for
loose fragments of bone, missed ethmoid partitions,
and points of bleeding.
• Wherever possible, any exposed bone is removed.
• Merocel spacers are placed for 24 h and removed on
postoperative day one when debridement occurs.

77. Postoperative management
• Surgery represents an adjunct to medical therapy in chronic
rhinosinusitis with nasal polyposis.
• Postoperatively, failure is almost assured if the ongoing
medical therapy to prevent recurrence is not administered.
• Routine postoperative debridement at first week of surgery
of the sinonasal cavity is critical to assuring success.
• Culturedirected antibiotics in the postoperative setting
should be utilized to limit iatrogenic infection, treat osteitis,
and eradicate sources of inflammation.

78. • Oral corticosteroid acts as a potent antiinflammatory in CRS with NP
• In diffuse nasal polyposis, the patient should be
discharged with a tapering course of prednisone
over a prolonged period, and overlapping
administration of topical corticosteroids should
begin before cessation of oral corticosteroids is
considered.
• Patients unwilling to undergo oral corticosteroid
therapy may benefit from topical administration
of budesonide 0.5 mg/2 mL mixed in 240 mL
normal saline for irrigation.

79. Other surgical techniques
• Nasalization procedure:
• The aim of the nasalisation procedure is to
remove the ethmoidal mucosa as completely as
possible without hazards, and to transform the
ethmoidal labyrinth into a unique cavity
opening into the nose.

80. • Aggressive Sinus Marsupialization Including the
Endoscopic Modified Lothrop Procedure:
• The frontal recess clearance maximizes the natural ostium
of the frontal sinus without enlarging it.
• The frontal drillout or EMLP creates the largest possible
frontal ostium diameter for individual anatomical
constraints.
• In patients who develop recurrent polyps after
surgery, the modified endoscopic Lothrop procedure, Draf
III or frontal drillout produces
better outcomes, and in some cases a cure, than standard
revision ESS.

81. Reasons for failure
•
•
•
•
•
•
•
•
•
•
Insufficient ethmoidectomy
Insufficient removal of septa
Insufficient drug concentration behind the septa
Insufficient cleaning of the polypoid mucosa behind the
septa
Pool for collection of secretions
Insufficient surgery of the frontal sinus
Polyps at the frontal recess and frontal ostium area
Polyps and mucoceles in the frontal sinus
Stenosis of frontal ostium
Insufficient surgery of the maxillary sinus

82. •
•
•
•
•
•
•
•
•
•
•
•
Insufficient maxillary sinus ostium
Reclosure of the ostium
Decreased ventilation and drainage
Insufficient drainage due to thick secretions
Insufficient cleaning preop and postop
Insufficient opening of anterior wall of sphenoid sinus
Decreased ventilation
Decreased drainage
Insufficient drug concentration
Insufficient cleaning preop and postop
Free bony spicles
Granulation tissue and polyp recurrence

83. Reference.
1. Scott- Brown otorhinolaryngology
2. Cummings Otolaryngology
3. Nasal polyposis by T. Metin Önerci
Berrylin J. Ferguson
4.Pubmed indexed Journals.

84. • THANK YOU
THANK YOU